Jasmonates (JAs) are signals in plant stress responses and development. One of the first observed and prominent responses to JAs is the induction of biosynthesis of different groups of secondary compounds. Among them are nicotine, isoquinolines, glucosinolates, anthocyanins, benzophenanthridine alkaloids, artemisinin, and terpenoid indole alkaloids (TIAs), such as vinblastine. This brief review describes modes of action of JAs in the biosynthesis of anthocyanins, nicotine, TIAs, glucosinolates and artemisinin. After introducing JA biosynthesis, the central role of the SCFCOI1-JAZ co-receptor complex in JA perception and MYB-type and MYC-type transcription factors is described. Brief comments are provided on primary metabolites as precursors of secondary compounds. Pathways for the biosynthesis of anthocyanin, nicotine, TIAs, glucosinolates and artemisinin are described with an emphasis on JA-dependent transcription factors, which activate or repress the expression of essential genes encoding enzymes in the biosynthesis of these secondary compounds. Applied aspects are discussed using the biotechnological formation of artemisinin as an example of JA-induced biosynthesis of secondary compounds in plant cell factories.

Plant microtubules form a highly dynamic
intracellular network with important roles for regulating cell division,
cell proliferation and cell morphology. Its organization and dynamics
are coordinated by various microtubule-associated proteins (MAPs) that
integrate environmental and developmental stimuli to fine-tune and
adjust cytoskeletal arrays. IQ67 DOMAIN (IQD) proteins recently emerged
as a class of plant-specific MAPs with largely unknown functions. Here,
using a reverse genetics approach, we characterize Arabidopsis IQD5 in
terms of its expression domains, subcellular localization and biological
functions. We show that IQD5 is expressed mostly in vegetative tissues,
where it localizes to cortical microtubule arrays. Our phenotypic
analysis of iqd5 loss-of-function lines reveals functions of IQD5 in
pavement cell (PC) shape morphogenesis. Histochemical analysis of cell
wall composition further suggests reduced rates of cellulose deposition
in anticlinal cell walls, which correlate with reduced anisotropic
expansion. Lastly, we demonstrate IQD5-dependent recruitment of
calmodulin calcium sensors to cortical microtubule arrays and provide
first evidence for important roles of calcium in regulation of PC
morphogenesis. Our work thus identifies IQD5 as a novel player in PC
shape regulation, and, for the first time, links calcium signaling to
developmental processes that regulate anisotropic growth in PCs.

Plant growth and development are a genetically
predetermined series of events but can change dramatically in response
to environmental stimuli, involving perpetual pattern formation and
reprogramming of development. The rate of growth is determined by cell
division and subsequent cell expansion, which are restricted and
controlled by the cell wall–plasma membrane–cytoskeleton continuum, and
are coordinated by intricate networks that facilitate intra- and
intercellular communication. An essential role in cellular signaling is
played by calcium ions, which act as universal second messengers that
transduce, integrate, and multiply incoming signals during numerous
plant growth processes, in part by regulation of the microtubule
cytoskeleton. In this review, we highlight recent advances in the
understanding of calcium-mediated regulation of microtubule-associated
proteins, their function at the microtubule cytoskeleton, and their
potential role as hubs in crosstalk with other signaling pathways.

Multicellular organisms rely upon the movement of signaling molecules across cells, tissues and organs to communicate among distal sites. In plants, herbivorous insects, necrotrophic pathogens and mechanical wounding stimulate the activation of the jasmonate (JA) pathway, which in turn triggers the transcriptional changes necessary to protect plants against those challenges, often at the expense of growth. Although previous evidence indicated that JA species can translocate from damaged into distal sites, the identity of the mobile compound(s), the tissues through which they translocate and the consequences of their relocation remain unknown. Here, we demonstrated that endogenous JA species generated after shoot injury translocate to unharmed roots via the phloem vascular tissue in Arabidopsis thaliana. By wounding wild-type shoots of chimeric plants and by quantifying the relocating compounds from their JA-deficient roots, we uncovered that the JA-Ile precursor 12-oxo-phytodienoic acid (OPDA) is a mobile JA species. Our data also showed that OPDA is a primary mobile compound relocating to roots where, upon conversion to the bioactive hormone, it induces JA-mediated gene expression and root growth inhibition. Collectively, our findings reveal the existence of long-distance transport of endogenous OPDA which serves as a communication molecule to coordinate shoot-to-root responses, and highlight the importance of a controlled distribution of JA species among organs during plant stress acclimation.

Inorganic phosphate (Pi) is often a limiting plant
nutrient. In members of the Brassicaceae family, such as Arabidopsis
(Arabidopsis thaliana), Pi deprivation reshapes root system architecture
to favor topsoil foraging. It does so by inhibiting primary root
extension and stimulating lateral root formation. Root growth inhibition
from phosphate (Pi) deficiency is triggered by iron-stimulated,
apoplastic reactive oxygen species generation and cell wall
modifications, which impair cell-to-cell communication and meristem
maintenance. These processes require LOW PHOSPHATE RESPONSE1 (LPR1), a
cell wall-targeted ferroxidase, and PHOSPHATE DEFICIENCY RESPONSE2
(PDR2), the single endoplasmic reticulum (ER)-resident P5-type ATPase
(AtP5A), which is thought to control LPR1 secretion or activity.
Autophagy is a conserved process involving the vacuolar degradation of
cellular components. While the function of autophagy is well established
under nutrient starvation (C, N, or S), it remains to be explored under
Pi deprivation. Because AtP5A/PDR2 likely functions in the ER stress
response, we analyzed the effect of Pi limitation on autophagy. Our
comparative study of mutants defective in the local Pi deficiency
response, ER stress response, and autophagy demonstrated that ER
stress-dependent autophagy is rapidly activated as part of the
developmental root response to Pi limitation and requires the genetic
PDR2-LPR1 module. We conclude that Pi-dependent activation of autophagy
in the root apex is a consequence of local Pi sensing and the associated
ER stress response, rather than a means for systemic recycling of the
macronutrient.

Electric signaling and Ca2+ waves were discussed
to occur in systemic wound responses. Two new overlapping scenarios were
identified: (i) membrane depolarization in two special cell types
followed by an increase in systemic cytoplasmic Ca2+ concentration
([Ca2+]cyt), and (ii) glutamate sensed by GLUTAMATE RECEPTOR LIKE
proteins and followed by Ca2+-based defense in distal leaves.

Plants face varying nutrient conditions, to which
they have to adapt to. Adaptive responses are nutrient-specific and
strategies to ensure supply and homeostasis for one nutrient might be
opposite to another one, as shown for phosphate (Pi) and iron (Fe)
deficiency responses, where many genes are regulated in an opposing
manner. This was also observed on the metabolite levels. Whereas root
and exudate levels of catechol-type coumarins, phenylpropanoid-derived
2-benzopyranones, which facilitate Fe acquisition, are elevated after Fe
deficiency, they are decreased after Pi deficiency. Exposing plants to
combined Pi and Fe deficiency showed that the generation of coumarin
profiles in Arabidopsis thaliana roots by Pi deficiency considerably
depends on the availability of Fe. Similarly, the effect of Fe
deficiency on coumarin profiles is different at low compared to high Pi
availability. These findings suggest a fine-tuning of coumarin profiles,
which depends on Fe and Pi availability. T-DNA insertion lines
exhibiting aberrant expression of genes involved in the regulation of Pi
starvation responses (PHO1, PHR1, bHLH32, PHL1, SPX1) and Fe starvation
responses (BRUTUS, PYE, bHLH104, FIT) were used to analyze the
regulation of the generation of coumarin profiles in Arabidopsis
thaliana roots by Pi, Fe, and combined Pi and Fe deficiency. The
analysis revealed a role of several Fe-deficiency response regulators in
the regulation of Fe and of Pi deficiency-induced coumarin profiles as
well as for Pi deficiency response regulators in the regulation of Pi
and of Fe deficiency-induced coumarin profiles. Additionally, the
regulation of Fe deficiency-induced coumarin profiles by Fe deficiency
response regulators is influenced by Pi availability. Conversely,
regulation of Pi deficiency-induced coumarin profiles by Pi deficiency
response regulators is modified by Fe availability.

Atypical myopathy (AM) in horses is caused by
ingestion of seeds of the Acer species (Sapindaceae family).
Methylenecyclopropylacetyl-CoA (MCPA-CoA), derived from hypoglycin A
(HGA), is currently the only active toxin in Acer pseudoplatanus or Acer
negundo seeds related to AM outbreaks. However, seeds or arils of
various Sapindaceae (e.g., ackee, lychee, mamoncillo, longan fruit) also
contain methylenecyclopropylglycine (MCPG), which is a structural
analogue of HGA that can cause hypoglycaemic encephalopathy in humans.
The active poison formed from MCPG is methylenecyclopropylformyl-CoA
(MCPF-CoA). MCPF-CoA and MCPA-CoA strongly inhibit enzymes that
participate in β-oxidation and energy production from fat. The aim of
our study was to investigate if MCPG is involved in Acer seed poisoning
in horses. MCPG, as well as glycine and carnitine conjugates
(MCPF-glycine, MCPF-carnitine), were quantified using high-performance
liquid chromatography-tandem mass spectrometry of serum and urine from
horses that had ingested Acer pseudoplatanus seeds and developed typical
AM symptoms. The results were compared to those of healthy control
horses. For comparison, HGA and its glycine and carnitine derivatives
were also measured. Additionally, to assess the degree of enzyme
inhibition of β-oxidation, several acyl glycines and acyl carnitines
were included in the analysis. In addition to HGA and the specific toxic
metabolites (MCPA-carnitine and MCPA-glycine), MCPG, MCPF-glycine and
MCPF-carnitine were detected in the serum and urine of affected horses.
Strong inhibition of β-oxidation was demonstrated by elevated
concentrations of all acyl glycines and carnitines, but the highest
correlations were observed between MCPF-carnitine and
isobutyryl-carnitine (r = 0.93) as well as between MCPA- (and MCPF-)
glycine and valeryl-glycine with r = 0.96 (and r = 0.87). As shown here,
for biochemical analysis of atypical myopathy of horses, it is
necessary to take MCPG and the corresponding metabolites into
consideration.

Jasmonic acid (JA) and its related derivatives are
ubiquitously occurring compounds of land plants acting in numerous
stress responses and development. Recent studies on evolution of JA and
other oxylipins indicated conserved biosynthesis. JA formation is
initiated by oxygenation of α-linolenic acid (α-LeA, 18:3) or 16:3 fatty
acid of chloroplast membranes leading to 12-oxo-phytodienoic acid
(OPDA) as intermediate compound, but in Marchantiapolymorpha and
Physcomitrellapatens, OPDA and some of its derivatives are final
products active in a conserved signaling pathway. JA formation and its
metabolic conversion take place in chloroplasts, peroxisomes and
cytosol, respectively. Metabolites of JA are formed in 12 different
pathways leading to active, inactive and partially active compounds. The
isoleucine conjugate of JA (JA-Ile) is the ligand of the receptor
component COI1 in vascular plants, whereas in the bryophyte M.
polymorpha COI1 perceives an OPDA derivative indicating its functionally
conserved activity. JA-induced gene expressions in the numerous biotic
and abiotic stress responses and development are initiated in a
well-studied complex regulation by homeostasis of transcription factors
functioning as repressors and activators.

Plant microtubules form a highly dynamic intracellular network with important roles for regulating cell division, cell proliferation and cell morphology. Its organization and dynamics are coordinated by various microtubule-associated proteins (MAPs) that integrate environmental and developmental stimuli to fine-tune and adjust cytoskeletal arrays. IQ67 DOMAIN (IQD) proteins recently emerged as a class of plant-specific MAPs with largely unknown functions. Here, using a reverse genetics approach, we characterize Arabidopsis IQD5 in terms of its expression domains, subcellular localization and biological functions. We show that IQD5 is expressed mostly in vegetative tissues, where it localizes to cortical microtubule arrays. Our phenotypic analysis of iqd5 loss-of-function lines reveals functions of IQD5 in pavement cell (PC) shape morphogenesis, as indicated by reduced interdigitation of neighboring cells in the leaf epidermis of iqd5 mutants. Histochemical analysis of cell wall composition further suggests reduced rates of cellulose deposition in anticlinal cell walls, which correlate with reduced asymmetric expansion. Lastly, we provide evidence for IQD5-dependent recruitment of calmodulin calcium sensors to cortical microtubule arrays. Our work thus identifies IQD5 as a novel player in PC shape regulation, and, for the first time, links calcium signaling to developmental processes that regulate multi-polar growth in PCs.